Defect of a complement receptor 3 epitope in a patient with systemic lupus erythematosus.

T Witte; F L Dumoulin; J E Gessner; J Schubert; O Götze; C Neumann; R F Todd; H Deicher; R E Schmidt

doi:10.1172/JCI116688

Abteilung Klinische Immunologie und Dermatologie, Medizinische Hochschule Hannover, Germany.

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Abteilung Klinische Immunologie und Dermatologie, Medizinische Hochschule Hannover, Germany.

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Abteilung Klinische Immunologie und Dermatologie, Medizinische Hochschule Hannover, Germany.

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Abteilung Klinische Immunologie und Dermatologie, Medizinische Hochschule Hannover, Germany.

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Abteilung Klinische Immunologie und Dermatologie, Medizinische Hochschule Hannover, Germany.

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Abteilung Klinische Immunologie und Dermatologie, Medizinische Hochschule Hannover, Germany.

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Abteilung Klinische Immunologie und Dermatologie, Medizinische Hochschule Hannover, Germany.

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Abteilung Klinische Immunologie und Dermatologie, Medizinische Hochschule Hannover, Germany.

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Abteilung Klinische Immunologie und Dermatologie, Medizinische Hochschule Hannover, Germany.

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Published in Volume 92, Issue 3 on September 1, 1993
J Clin Invest. 1993;92(3):1181–1187. https://doi.org/10.1172/JCI116688.
© 1993 The American Society for Clinical Investigation

Published September 1, 1993 - Version history

Complement receptor 3 (CR3) is expressed on cells of the reticuloendothelial system and involved in the clearance of immune complexes. In this article a patient with a deficiency of the C3bi binding site of this receptor is described. Clinically this patient exhibited predominantly cutaneous manifestations of a systemic lupus erythematosus with an immune vasculitis and panniculitis. The deficiency of the CR3 epitope was demonstrated using flow cytometry. The functional relevance of this defect was demonstrated in a rosetting assay with C3bi-loaded erythrocytes. C3bi binding was found to be significantly decreased. Furthermore, there was an impairment of phagocytosis of opsonized Escherichia coli. The CR3 defect is not due to an autoantibody but is assumed to have a genetic basis. These data suggest that the defect of the CR3 may be involved in the pathogenesis of the immune vasculitis in this patient.

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Defect of a complement receptor 3 epitope in a patient with systemic lupus erythematosus.

T Witte, F L Dumoulin, J E Gessner, J Schubert, O Götze, C Neumann, R F Todd 3rd, H Deicher, and R E Schmidt

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Defect of a complement receptor 3 epitope in a patient with systemic lupus erythematosus.

T Witte, F L Dumoulin, J E Gessner, J Schubert, O Götze, C Neumann, R F Todd 3rd, H Deicher, and R E Schmidt

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